The effect of SATB2 expression on chromatin organization in BEAS2B lung epithelial cells [RNA-seq; SATB2 overexpression]

Thus, it is still unclear if non-genetic mechanisms are sufficient to trigger malignant transformation. Chronic, low-dose exposure to inorganic arsenic is known to cause lung malignancies, yet arsenic at low levels does not induce point mutations.

Here, we show iAs upregulates Special AT-rich binding protein 2 (SATB2), a chromatin organizer that reprograms cell-specific and/or developmentally-sensitive gene networks, to drive mutant KRAS-like gene expression patterns during arsenic-mediated transformation of BEAS2B cells. Thus, oncogenic pathways can be activated in mammalian cells without pre-disposing mutations in oncogenes or epigenetic regulators.